The role of gastrin in production of gastric acid hypersecretion associated with duodenal ulcer disease will be examined by comparing gastric secretory response and changes in circulating gastrin during intravenous infusion of pure hormone with changes in circulating gastrin observed after a protein meal is eaten by the same subjects. This type of meal is known to elicit near maximal rates of acid secretion. The major question is whether gastrin is the major regulator of gastric acid secretion and whether its effect in ulcer subjects is abnormal. Gastrin exists in tissues and in the circulation in several forms. We have found that the most potent form, G-17, is less abundant than G-34 in the circulation but probably is the major physiologically active form. Thus it will be necessary to separate different molecular forms and measure them separately. This will be done by means of a combination of column chromatography and radioimmunoassay. Purified human gastrins will be given by infusion to mimic the blood concentrations achieved after a meal. Sensitivity to different exogenous forms of gastrin and endogenous release of gastrin will be compared in normal and ulcer subjects to see if some defect can be identified in ulcer subjects which would account for the higher average rates of acid secretion found in these patients.